Gene Control of Programmed Myocardial Cell Death in Acute Myocardial Infarction, Its Dynamics in Treatment and Prospects for Therapy
The aim of the investigation was to study gene regulation of apoptosis in acute myocardial infarction and during the treatment, and assess the effect of levocarnitine (Elcar) on gene expression of Fas-dependent apoptosis.
Materials and Methods. We examined 28 patients with Q-myocardial infarction included in the study within the first 24 h of the disease and followed up during the treatment course. The patients were divided into two groups: group 1 (n=10) consisted of patients with standard treatment (anti-aggregants, ACE inhibitors, and anti-anginal agents — if indicated); group 2 (n=18) — those patients, who received standard treatment with Elcar (levocarnitine) intravenously, in 5% glucose normal saline, at the dose of 3.0 g a day for three days. For the following 7 days the patients were given Elcar per os, 4.0 g a day. A control group (group 3) (n=18) consisted of healthy subjects.
All patients underwent general examination, ECG, echocardiography, genetic research: we determined mRNA gene expression of mFas and sFas using real-time polymerase chain reaction thrice in each patient — on admission, after 1 week treatment, and at the end of the second week of treatment.
Results. Apoptotic gene expression in patients with Q-infarction was found to be increased compared to the norm, the increase lasting for a longer period than acute myocardial infarction itself. This fact enables to explain the cause of prolonged apoptosis by the sustained activity of apoptosis-inducing genes. The use of levocarnitine promotes the normalization of an increased level of gene expression, and has a cardioprotective effect that is important in acute myocardial infarction treatment.
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